Dept. of Psychology, Wilfrid Laurier University, Waterloo, ON N2L 3C5, Canada.
Neuropharmacology. 2012 Mar;62(4):1627-33. doi: 10.1016/j.neuropharm.2011.11.025. Epub 2011 Dec 13.
It is well known that antidepressants both improve mood and increase the rate at which the dentate gyrus (DG) generates new neurons. In addition to the implications of neurogenesis for mood regulation, the production and survival of granule cells has also been implicated in learning and memory. Despite this evidence, the results of studies on the effect of antidepressants on memory have been mixed. A critical piece of data that may be missing from previous studies, however, is insight into (a) the location that newborn neurons migrate to following fluoxetine administration and (b) their ability to express normal patterns of activity-related genes. Here we demonstrate a finding that may resolve the discrepancy in the effects fluoxetine-induced neurogenesis on mood and memory: after 5 weeks delay, the net additional neurons generated in animals given the antidepressant fluoxetine during treatment are functionally normal, but preferentially accumulate (due to changes in migration and/or survival) in an area of the DG that is not recruited by spatial memory tasks.
众所周知，抗抑郁药既能改善情绪，又能提高齿状回（DG）产生新神经元的速度。除了神经发生对情绪调节的影响外，颗粒细胞的产生和存活也与学习和记忆有关。尽管有这些证据，但关于抗抑郁药对记忆影响的研究结果却喜忧参半。然而，以前的研究可能缺少一个关键数据，即缺乏对抗抑郁药给药后新生神经元迁移位置的深入了解（a）和它们表达正常活动相关基因模式的能力（b）。在这里，我们展示了一个可能解决氟西汀诱导的神经发生对情绪和记忆影响不一致的发现：在 5 周的延迟后，在治疗期间给予抗抑郁药氟西汀的动物中产生的额外神经元数量净增加，功能正常，但由于迁移和/或存活的变化而优先积累（due to changes in migration and/or survival）在 DG 的一个区域，该区域不能被空间记忆任务招募。
